Cigarette smoking hinders human periodontal ligament-derived stem cell proliferation, migration and differentiation potentials.

Autor: Ng TK; Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong., Huang L; Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong., Cao D; Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong., Yip YW; Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong., Tsang WM; Oral Maxillofacial Surgery and Dentistry, North District Hospital, Hong Kong., Yam GH; Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong., Pang CP; Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Hong Kong., Cheung HS; 1] Geriatric Research, Education and Clinical Center, Miami Veterans Affairs Medical Center, Miami, FL, United States [2] Department of Biomedical Engineering, University of Miami, Coral Gables, FL, United States.
Jazyk: angličtina
Zdroj: Scientific reports [Sci Rep] 2015 Jan 16; Vol. 5, pp. 7828. Date of Electronic Publication: 2015 Jan 16.
DOI: 10.1038/srep07828
Abstrakt: Cigarette smoking contributes to the development of destructive periodontal diseases and delays its healing process. Our previous study demonstrated that nicotine, a major constituent in the cigarette smoke, inhibits the regenerative potentials of human periodontal ligament-derived stem cells (PDLSC) through microRNA (miRNA) regulation. In this study, we hypothesized that the delayed healing in cigarette smokers is caused by the afflicted regenerative potential of smoker PDLSC. We cultured PDLSC from teeth extracted from smokers and non-smokers. In smoker PDLSC, we found significantly reduced proliferation rate and retarded migration capabilities. Moreover, alkaline phosphatase activity, calcium deposition and acidic polysaccharide staining were reduced after BMP2-induced differentiation. In contrast, more lipid deposition was observed in adipogenic-induced smoker PDLSC. Furthermore, two nicotine-related miRNAs, hsa-miR-1305 (22.08 folds, p = 0.040) and hsa-miR-18b (15.56 folds, p = 0.018), were significantly upregulated in smoker PDLSC, suggesting these miRNAs might play an important role in the deteriorative effects on stem cells by cigarette smoke. Results of this study provide further evidences that cigarette smoking affects the regenerative potentials of human adult stem cells.
Databáze: MEDLINE